Eleutheroside B, a compound from Siberian ginseng, dramatically reduced amyloid-beta and tau protein accumulation while improving cognition and lifespan in transgenic C. elegans worms modeling Alzheimer's disease. The compound activated three key stress-response pathways (skn-1, daf-16, hsf-1), boosted antioxidant enzymes SOD-3 and GST-4, and crucially triggered autophagy—the cellular cleanup process that removes damaged proteins. When researchers knocked down autophagy genes like aak-2 and lgg-1, eleutheroside B's protective effects vanished, confirming autophagy as the primary mechanism. This finding positions eleutheroside B within the growing recognition that enhancing autophagy represents a promising therapeutic avenue for neurodegenerative diseases. The dual action—simultaneously reducing oxidative stress while promoting protein clearance—mirrors the approach of leading longevity interventions like rapamycin and fasting mimetics. However, the C. elegans model, while valuable for mechanistic insights, has significant limitations for human translation. Worms lack the complex brain architecture where Alzheimer's manifests, and many compounds showing promise in simple organisms fail in mammals. Still, the robust activation of evolutionarily conserved pathways suggests eleutheroside B warrants investigation in higher-order models, particularly given its apparent safety profile even at high doses.